The proposed work is aimed at an elucidation of the phenomenon of retinal light-damage. It is suggested that this damage is an exaggeration of normal light-adaptation. The crux of this hypothesis is the fact that constant light causes a reduction of aerobic metabolism in receptors and a shift toward pentose shunt path without concomitant decrease in cellular demand for high-energy phosphates. It is proposed that damage results if the receptor are continuously deprived of these aerobic mechanisms by the constant light. This implies that damage and normal adaptation are part of a continuum and a major portion of the proposed work deals with an empirical demonstration of this. Rhodopsin content, ERG threshold, pupillometry and histology (light microsocope level) will be used as monitors of the light damage and recovery from it. The second major part of the work deals with a demonstration, at the molecular level, that degree of damage correlates with the rate of biosynthesis of individual molecules and rod receptor discs. It is predicted that light "adapted-damaged" rats will show slower rates of incorporation of protein and lipid precursors than normal animals.